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1 xpression of the full virulence potential of BHV-5.
2  with the gE5 epitope-reverted and wild-type BHV-5.
3  with the gE5 epitope-reverted and wild-type BHV-5.
4  similar to that of the Us9 rescue mutant of BHV-5.
5  differential neuropathogenesis of BHV-1 and BHV-5.
6 te genomic sequence of bovine herpesvirus 5 (BHV-5), an alphaherpesvirus responsible for fatal mening
7 ted BHV-1 and BHV-5 recombinants: gE-deleted BHV-5 (BHV-5gEDelta), BHV-5 expressing BHV-1 gE (BHV-5gE
8 nfected intranasally with gE epitope-deleted BHV-5 did not develop seizures, and only 20% of the infe
9 tranasal infection, the Us9 rescue mutant of BHV-5 displayed a wild-type level of neurovirulence and
10 combinants: gE-deleted BHV-5 (BHV-5gEDelta), BHV-5 expressing BHV-1 gE (BHV-5gE1), and BHV-1 expressi
11                        Rabbits infected with BHV-5 expressing BHV-1 Us9 showed severe neurological si
12       In a rabbit seizure model, Us9-deleted BHV-5 failed to invade the central nervous system (CNS)
13                       The gE epitope-deleted BHV-5 formed wild-type-sized plaques in MDBK cells, and
14 ng BHV-1 gE (BHV-5gE1), and BHV-1 expressing BHV-5 gE (BHV-1gE5).
15 tion, and immunohistochemistry indicate that BHV-5 gE is important for efficient neural spread and ne
16                                     However, BHV-5 gE is not required for initial viral entry into ol
17  predicted amino acid sequences of BHV-1 and BHV-5 gE open reading frames showed that they had 72% id
18 ificantly less efficiently in the brain than BHV-5 gE revertant or wild-type BHV-5, which produced se
19                    The bovine herpesvirus 5 (BHV-5) gE ectodomain contains a glycine-rich epitope cod
20                    Intranasal inoculation of BHV-5 gEDelta and BHV-5gE1 produced significantly reduce
21 ompared with those of a Us9 rescue mutant of BHV-5 in a rabbit model.
22  significantly reduced the neurovirulence of BHV-5 in rabbits.
23 a doublet of 17- and 19-kDa protein bands in BHV-5-infected cell lysates and in purified virions.
24  anterograde spread of bovine herpesvirus 5 (BHV-5) infection from the olfactory receptor neurons to
25                                              BHV-5 is very similar to BHV-1, the etiological agent of
26                        Bovine herpesvirus 5 (BHV-5) is a neurovirulent alphaherpesvirus that causes f
27                         The structure of the BHV-5 latency-related (LR) region departs markedly from
28  determine the role of the BHV-5 Us9 gene in BHV-5 neuropathogenesis, a BHV-5 Us9 deletion recombinan
29 it is likely these differences contribute to BHV-5 neuropathogenicity.
30 V-1 and BHV-5, we have constructed BHV-1 and BHV-5 recombinants: gE-deleted BHV-5 (BHV-5gEDelta), BHV
31 d BICP22, the three proteins being longer in BHV-5 than in BHV-1.
32 erences, BHV-1 Us9 not only complemented for BHV-5 Us9 and rescued the anterograde-spread defect of t
33 BHV-5 Us9 gene in BHV-5 neuropathogenesis, a BHV-5 Us9 deletion recombinant was generated and its neu
34                 To determine the role of the BHV-5 Us9 gene in BHV-5 neuropathogenesis, a BHV-5 Us9 d
35                                          The BHV-5 Us9 gene sequence was determined, and the predicte
36 9 is a 30- to 32-kDa protein, whereas mature BHV-5 Us9 is an 18- to 20-kDa protein.
37 xpressed at 3 h postinfection (hpi), whereas BHV-5 Us9 is expressed at 6 hpi.
38                                              BHV-5 Us9 peptide-specific antibody recognized a doublet
39 ed, and the predicted amino acid sequence of BHV-5 Us9 was compared with the corresponding Us9 sequen
40 rescued the anterograde-spread defect of the BHV-5 Us9-deleted virus but conferred increased neurovir
41 earlier than BHV-5 wild-type or Us9-reverted BHV-5 virus.
42 tory pathway, but the Us9 deletion mutant of BHV-5 was virtually avirulent and failed to invade the C
43 e of the neurovirulent bovine herpesvirus 5 (BHV-5) was determined and compared with that of the nonn
44  differential neuropathogenesis of BHV-1 and BHV-5, we have constructed BHV-1 and BHV-5 recombinants:
45 e brain than BHV-5 gE revertant or wild-type BHV-5, which produced severe neurological signs in 70 to
46 nfection, which was 1 to 2 days earlier than BHV-5 wild-type or Us9-reverted BHV-5 virus.
47                               In contrast to BHV-5, wild-type BHV-1 failed to invade the CNS followin

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